<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Manson JJ</submitter><funding>Versus Arthritis</funding><funding>Medical Research Council</funding><funding>National Institute for Health Research (NIHR)</funding><funding>Vivensa Foundation</funding><funding>Rosetrees</funding><funding>Multiple Sclerosis Society</funding><funding>Wellcome Trust</funding><funding>Academy of Medical Sciences</funding><pagination>e594-e602</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7442426</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>2(10)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>A subset of patients with severe COVID-19 develop a hyperinflammatory syndrome, which might contribute to morbidity and mortality. This study explores a specific phenotype of COVID-19-associated hyperinflammation (COV-HI), and its associations with escalation of respiratory support and survival.&lt;h4>Methods&lt;/h4>In this retrospective cohort study, we enrolled consecutive inpatients (aged ≥18 years) admitted to University College London Hospitals and Newcastle upon Tyne Hospitals in the UK with PCR-confirmed COVID-19 during the first wave of community-acquired infection. Demographic data, laboratory tests, and clinical status were recorded from the day of admission until death or discharge, with a minimum follow-up time of 28 days. We defined COV-HI as a C-reactive protein </pubmed_abstract><journal>The Lancet. Rheumatology</journal><pubmed_title>COVID-19-associated hyperinflammation and escalation of patient care: a retrospective longitudinal cohort study.</pubmed_title><pmcid>PMC7442426</pmcid><funding_grant_id>21226</funding_grant_id><funding_grant_id>MC_PC_15005</funding_grant_id><funding_grant_id>RPGF1902/117</funding_grant_id><funding_grant_id>211153/Z/18/Z</funding_grant_id><funding_grant_id>ACF-2018-01-004</funding_grant_id><funding_grant_id>20164</funding_grant_id><funding_grant_id>RPGF1902\117</funding_grant_id><funding_grant_id>21593</funding_grant_id><funding_grant_id>ACF-2018-01-001</funding_grant_id><funding_grant_id>CL-2013-01-003</funding_grant_id><funding_grant_id>22203</funding_grant_id><funding_grant_id>076</funding_grant_id><funding_grant_id>M409-F1</funding_grant_id><funding_grant_id>CL-2017-01-004</funding_grant_id><funding_grant_id>M409</funding_grant_id><funding_grant_id>NIHR-INF-0958</funding_grant_id><funding_grant_id>ACF-2016-18-026</funding_grant_id><funding_grant_id>AMS-SGCL11-Duncan</funding_grant_id><pubmed_authors>West J</pubmed_authors><pubmed_authors>Mehta P</pubmed_authors><pubmed_authors>Rampling T</pubmed_authors><pubmed_authors>Tattersall RS</pubmed_authors><pubmed_authors>Hanrath AT</pubmed_authors><pubmed_authors>J'Bari H</pubmed_authors><pubmed_authors>Williams B</pubmed_authors><pubmed_authors>Lendrem BC</pubmed_authors><pubmed_authors>Robinson GA</pubmed_authors><pubmed_authors>Schim van der Loeff I</pubmed_authors><pubmed_authors>Naja M</pubmed_authors><pubmed_authors>Crooks C</pubmed_authors><pubmed_authors>Duncan CJA</pubmed_authors><pubmed_authors>De Soyza A</pubmed_authors><pubmed_authors>Luintel A</pubmed_authors><pubmed_authors>Peckham H</pubmed_authors><pubmed_authors>Goulden B</pubmed_authors><pubmed_authors>Baker KF</pubmed_authors><pubmed_authors>Manson JJ</pubmed_authors><pubmed_authors>Ledlie A</pubmed_authors><pubmed_authors>Liddle T</pubmed_authors><pubmed_authors>Ribeiro Santos L</pubmed_authors><pubmed_authors>Khan E</pubmed_authors><pubmed_authors>Waddington KE</pubmed_authors><pubmed_authors>Marks M</pubmed_authors><pubmed_authors>Hawkins E</pubmed_authors><pubmed_authors>Collin M</pubmed_authors><pubmed_authors>Adeney C</pubmed_authors><pubmed_authors>Brown M</pubmed_authors><pubmed_authors>Singer M</pubmed_authors><pubmed_authors>Snell A</pubmed_authors><pubmed_authors>McLoughlin E</pubmed_authors><pubmed_authors>Greenwood M</pubmed_authors><pubmed_authors>Martin-Gutierrez L</pubmed_authors><pubmed_authors>Peng J</pubmed_authors><pubmed_authors>Jury EC</pubmed_authors></additional><is_claimable>false</is_claimable><name>COVID-19-associated hyperinflammation and escalation of patient care: a retrospective longitudinal cohort study.</name><description>&lt;h4>Background&lt;/h4>A subset of patients with severe COVID-19 develop a hyperinflammatory syndrome, which might contribute to morbidity and mortality. This study explores a specific phenotype of COVID-19-associated hyperinflammation (COV-HI), and its associations with escalation of respiratory support and survival.&lt;h4>Methods&lt;/h4>In this retrospective cohort study, we enrolled consecutive inpatients (aged ≥18 years) admitted to University College London Hospitals and Newcastle upon Tyne Hospitals in the UK with PCR-confirmed COVID-19 during the first wave of community-acquired infection. Demographic data, laboratory tests, and clinical status were recorded from the day of admission until death or discharge, with a minimum follow-up time of 28 days. We defined COV-HI as a C-reactive protein </description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Oct</publication><modification>2026-05-03T22:51:57.376Z</modification><creation>2020-08-29T07:28:18Z</creation></dates><accession>S-EPMC7442426</accession><cross_references><pubmed>32864628</pubmed><doi>10.1016/S2665-9913(20)30275-7</doi></cross_references></HashMap>